Rare Variants in PLD3 Do Not Affect Risk for Early‐Onset Alzheimer Disease in a European Consortium Cohort

نویسندگان

  • Rita Cacace
  • Tobi Van den Bossche
  • Sebastiaan Engelborghs
  • Nathalie Geerts
  • Annelies Laureys
  • Lubina Dillen
  • Caroline Graff
  • Håkan Thonberg
  • Huei‐Hsin Chiang
  • Pau Pastor
  • Sara Ortega‐Cubero
  • Maria A. Pastor
  • Janine Diehl‐Schmid
  • Panagiotis Alexopoulos
  • Luisa Benussi
  • Roberta Ghidoni
  • Giuliano Binetti
  • Benedetta Nacmias
  • Sandro Sorbi
  • Raquel Sanchez‐Valle
  • Albert Lladó
  • Ellen Gelpi
  • Maria Rosário Almeida
  • Isabel Santana
  • Magda Tsolaki
  • Maria Koutroumani
  • Jordi Clarimon
  • Alberto Lleó
  • Juan Fortea
  • Alexandre de Mendonça
  • Madalena Martins
  • Barbara Borroni
  • Alessandro Padovani
  • Radoslav Matej
  • Zdenek Rohan
  • Mathieu Vandenbulcke
  • Rik Vandenberghe
  • Peter P. De Deyn
  • Patrick Cras
  • Julie van der Zee
  • Kristel Sleegers
  • Christine Van Broeckhoven
چکیده

Rare variants in the phospholipase D3 gene (PLD3) were associated with increased risk for late-onset Alzheimer disease (LOAD). We identified a missense mutation in PLD3 in whole-genome sequence data of a patient with autopsy confirmed Alzheimer disease (AD) and onset age of 50 years. Subsequently, we sequenced PLD3 in a Belgian early-onset Alzheimer disease (EOAD) patient (N = 261) and control (N = 319) cohort, as well as in European EOAD patients (N = 946) and control individuals (N = 1,209) ascertained in different European countries. Overall, we identified 22 rare variants with a minor allele frequency <1%, 20 missense and two splicing mutations. Burden analysis did not provide significant evidence for an enrichment of rare PLD3 variants in EOAD patients in any of the patient/control cohorts. Also, meta-analysis of the PLD3 data, including a published dataset of a German EOAD cohort, was not significant (P = 0.43; OR = 1.53, 95% CI 0.60-3.31). Consequently, our data do not support a role for PLD3 rare variants in the genetic etiology of EOAD in European EOAD patients. Our data corroborate the negative replication data obtained in LOAD studies and therefore a genetic role of PLD3 in AD remains to be demonstrated.

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عنوان ژورنال:

دوره 36  شماره 

صفحات  -

تاریخ انتشار 2015